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A complete set of vocabulary flashcards covering drug classes, mechanisms of action, and examples from the HNN215 Drug Portfolio lecture notes.
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ACE Inhibitors
Antihypertensive drugs (e.g., Perindopril, Ramipril) that block the conversion of angiotensin I to angiotensin II and inhibit the breakdown of bradykinin.
Aminoglycosides
Bactericidal antibiotics (e.g., Gentamycin) that prevent protein synthesis by binding to the 30s ribosomal subunit, causing cell membrane damage.
Antacids
Weak bases like Aluminium hydroxide that neutralize hydrochloric acid secreted by parietal cells to treat abdominal discomfort.
Anticholinergics
Drugs (e.g., Ipratropium) that promote bronchodilation by preventing acetylcholine from binding to muscarinic receptors, blocking the PNS response.
Beta2 Agonists
Medications (e.g., Salbutamol, Salmeterol) that relax bronchial smooth muscle by stimulating beta2 adrenoreceptors.
Beta Blockers
Antiarrhythmic agents (e.g., Metoprolol, Labetalol) that block beta receptors in the heart, peripheral vasculature, bronchi, and kidneys.
Beta Lactams
Bactericidal antibiotics (e.g., Penicillin, Cephalosporin) that interfere with bacterial cell wall synthesis by binding to penicillin-binding proteins.
Biguanides
Diabetes medication (Metformin) that reduces glucose production in the liver and increases insulin sensitivity.
Bulk-forming laxatives
Laxatives like Psyllium (Metamucil) that absorb water in the colon to increase faecal bulk and stimulate peristalsis.
Calcium Channel Blockers
Antihypertensives (e.g., Amlodipine, Verapamil) that block the inward movement of calcium into vascular smooth muscle, myocardium, and the cardiac conducting system.
Cardiac Glycoside
Digoxin; increases intracellular calcium to increase myocardial contraction force while slowing heart rate and AV nodal conduction.
Corticosteroids (systemic)
Drugs like Hydrocortisone and Prednisolone that reduce inflammation by decreasing the production of inflammatory mediators.
Corticosteroids (inhaled)
Anti-inflammatory agents (e.g., Fluticasone) that alter intracellular protein synthesis to regulate cell inflammation.
Dopamine-2 Antagonist
Antiemetics such as Metoclopramide that block dopamine receptors in the medulla and GIT to prevent nausea and vomiting.
Glycopeptides
Bactericidal antibiotics like Vancomycin that inhibit bacterial cell wall synthesis; associated with 'Red man' syndrome during rapid infusion.
Heparins
Anticoagulants (e.g., Enoxaparin) that inactivate clotting factors IIa (thrombin) and Xa by binding to antithrombin III.
Histamine-2 receptor antagonists
Drugs like Ranitidine and Famotidine that competitively block H2 receptors on parietal cells to reduce gastric acid secretion.
Insulins
Hormonal treatments (e.g., Novorapid, Lantus) that restore the ability to metabolize glucose by enhancing cellular glucose uptake.
Local anaesthetics (Amides)
Agents like Lidocaine that reversibly disrupt impulse conduction in peripheral nerves by blocking sodium ion channels.
Loop diuretics
Potent diuretics (e.g., Furosemide) that inhibit reabsorption of sodium and chloride in the ascending portion of the loop of Henle.
Macrolides
Bacteriostatic antibiotics (e.g., Erythromycin) that inhibit bacterial protein synthesis by binding to the 50s ribosomal subunit.
Neuraminidase inhibitor
Oseltamivir; inhibits the neuraminidase surface protein to prevent the release of the influenza virus from host cells.
Nitrates
Vasodilators like Glyceryl trinitrate (GTN) that provide an exogenous source of nitric oxide to reduce venous return and myocardial oxygen requirements.
Non-opioid analgesics
Paracetamol; inhibits prostaglandin synthesis in the CNS and modulates descending pathways to provide analgesia.
Non-steroidal anti-inflammatory drugs (NSAIDs)
Drugs (e.g., Ibuprofen, Celecoxib) that inhibit prostaglandin production by inhibiting cyclo-oxygenase.
Oestrogen receptor modulators
Hormonal anticancer drugs like Tamoxifen that compete with oestrogen for receptor sites in breast tissue to slow tumor growth.
Opioid analgesics
Analgesics (e.g., Morphine, Fentanyl) that act on receptors in the CNS and GIT to reduce transmission of pain impulses.
Osmotic laxatives
Laxatives like Lactulose containing poorly absorbed sugars or salts that draw water into the intestines to stimulate peristalsis.
Polyene (anti-fungal)
Nystatin; binds to ergosterol in fungal cell membranes, causing leakage of intracellular components.
Proton Pump Inhibitors
Drugs (e.g., Esomeprazole, Pantoprazole) that bind to the proton pump of parietal cells to inhibit acid secretion.
Stimulant laxatives
Senna; provides direct stimulation of nerve endings in the colon to increase intestinal motility.
Stool softeners
Docusate; a substance that assists water to mix with faeces to soften the stool, typically taking 1-3 days for onset.
Sulfonylureas
Diabetes medications like Gliclazide that increase the secretion of insulin from pancreatic beta cells.
Sympathomimetics
Adrenaline; a drug used in anaphylaxis to stimulate the sympathetic nervous system.
Thiazide and related diuretics
Diuretics (e.g., Indapamide) that inhibit sodium and chloride reabsorption in the proximal segment of the distal convoluted tubule.
Warfarin
A vitamin K antagonist that inhibits the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X).
5HT3 Antagonist
Antiemetics like Ondansetron that block serotonin receptors in the medulla and GIT; particularly effective for chemotherapy-induced nausea.
Half-life
Time interval required for elimination processes to reduce the concentration of a medication in the body by half.
Steady state concentration
Where the rate of medication administration is equal to the rate of medication elimination, thus maintaining the concentration of the drug above the minimum effective concentration.
Therapeutic range
Concentration of medication between the minimum level and toxic level.
Bolus dose
A mass intended for IV injection over a short period of time to quickly achieve therapeutic concentration within the body.
Agonist
Medication capable of binding to receptors to initiate medication actions.
Antagonist
Agent that blocks receptors, stopping what normally binds to the receptor, and as a result inhibits normal response.
Pharmacodynamics
The biochemical and physiological effects of medications, study of the mechanism of action/how the drug works on the body.
Pharmacokinetics
Study of the absorption, distribution, metabolism, and elimination of medications; what the body does to the medication.
Duration of Action
The length of time for which the medication has a pharmacological effect. Measured from onset of action to the time when it drops below minimum effective concentration.
Onset of action
Begins when the medication enters the plasma.